Presenter Information

Session Number

Session 1F: 4th Presentation

Advisor(s)

Vandana Chinwalla, Illinois Mathematics and Science Academy

Location

Room A115

Start Date

28-4-2017 8:30 AM

End Date

28-4-2017 9:45 AM

Abstract

Cancer remains a major cause of death around the world despite the significant progress made through research in targeted therapies and understanding of the biology of cancer. Mixed Lineage Leukemia (MLL) gene is linked to various cancers but is especially known for causing a variety of childhood leukemias. Also known as KMT2A, MLL is a chromatin modifier that modifies the chromatin structure via its methyltransferase activity, controlling expression of genes involved in embryogenesis and hematopoiesis. Alteration in MLL often leads to tumorigenesis due to misexpression of MLL-controlled HOX genes which may play a central role in oncogenesis. However, at least one copy of normal MLL is shown to be necessary for tumorigenesis. We aim to utilize the gene-editing capabilities of CRISPR/Cas9 to knock out MLL in MCF-7 breast-cancer cells. We designed MLL-gRNA-CRISPR/Cas9 construct to target mutations at the 5’ end of MLL genomic DNA to knock out the expression. The first transfection of MCF- 7 cells with our CRISPR/Cas9 construct, yielded a decrease in cell proliferation compared to the control. Given these preliminary results, we aim to test CRISPR/Cas9 on various cancers in order to validate MLL’s role as a cause for cancer.

Share

Cancer remains a major cause of death around the world despite the significant progress made through research in targeted therapies and understanding of the biology of cancer. Mixed Lineage Leukemia (MLL) gene is linked to various cancers but is especially known for causing a variety of childhood leukemias. Also known as KMT2A, MLL is a chromatin modifier that modifies the chromatin structure via its methyltransferase activity, controlling expression of genes involved in embryogenesis and hematopoiesis. Alteration in MLL often leads to tumorigenesis due to misexpression of MLL-controlled HOX genes which may play a central role in oncogenesis. However, at least one copy of normal MLL is shown to be necessary for tumorigenesis. We aim to utilize the gene-editing capabilities of CRISPR/Cas9 to knock out MLL in MCF-7 breast-cancer cells. We designed MLL-gRNA-CRISPR/Cas9 construct to target mutations at the 5’ end of MLL genomic DNA to knock out the expression. The first transfection of MCF- 7 cells with our CRISPR/Cas9 construct, yielded a decrease in cell proliferation compared to the control. Given these preliminary results, we aim to test CRISPR/Cas9 on various cancers in order to validate MLL’s role as a cause for cancer.